Adenosine and the acid-base state of vascular smooth muscle.
Hog carotid artery media was incubated under conditions of normocapnia (95% O2-5% CO2) and hypercapnia (nominally 75% O2-25%CO2). The intracellular pH (pHi) was determined from the distribution of 14C-labeled 5,5-dimethyloxazoladine-2,4-dione, alpha- and beta-receptor antagonists were used to block the effects of endogenous catecholamines. With 5% CO2, adenosine had no effect on the pHi. High K+ (25mM) and dipyridamole (DPM) induced a cellular metabolic acidosis that was reversed by adenosine and not affected by 0.5 mM ca2+ or ouabain. Hypercapnia decreased the resting pHi from 7.30 to 6.79. Adenosine significantly attenuated this decrease. With high K+ or DPM, a similar degree of hypercapnia only depressed the pHi to 6.91 and 6.90, respectively. The alkalinizing effect of high K+ and DPM was not altered by 0.5 mM Ca2+, was partically reversed by ouabain, and was completely reversed by adenosine. These results suggest that, under normocapnic conditions, although adenosine relaxes the contraction associated with K+-depolarization, it does not do so by elevating cellular proton levels. However, adenosine may decrease a tissue's ability to attenuate a local respiratory acidosis characteristic of increased O2 demand, resulting in relaxation under hypercapnic conditions. In any case, this demonstrates an interaction, with respect to the acid-base state of the vascular smooth muscle cells, among adenosine, K+, and H+, all suggested components of the metabolic theory of blood flow autoregulation.
D000136:Acid-Base Equilibrium; D000241:Adenosine / Q000502:physiology*; D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D007424:Intracellular Fluid / Q000502:physiology; D009119:Muscle Contraction; D009126:Muscle Relaxation; D009130:Muscle, Smooth / Q000378:metabolism*; D010313:Partial Pressure; D013552:Swine
D002245:Carbon Dioxide; D000241:Adenosine